Signa Vitae. 2025; 21(12): 107-113. doi: 10.22514/sv.2025.194
Original Research

Frontal QRS-T angle and mortality in ischemic stroke patients: a multicenter study

Murat Genç1,*,, Didem Çankaya Gökdere2, Adil Emre Gezer3, Melih Çamcı4, Bensu Bulut5, Medine Akkan Öz6, Ramiz Yazıcı7, Huseyin Mutlu8, Zekeriya Uykan9

1Department of Emergency Medicine, Ankara Training and Research Hospital, 06230 Ankara, Turkey

2Department of Emergency Medicine, Bodrum State Hospital, 48480 Muğla, Turkey

3Department of Emergency Medicine, Ankara Etlik City Hospital, 06170 Ankara, Turkey

4Department of Emergency Medicine, Ankara Bilkent City Hospital, Yıldırım Beyazıt University, 06800 Ankara, Turkey

5Department of Emergency Medicine, Ankara Gulhane Training and Research Hospital, Health Science University, 06010 Ankara, Turkey

6Department of Emergency Medicine, Ankara Gulhane Training and Research Hospital, 06010 Ankara, Turkey

7Department of Emergency Medicine, Istanbul Kanuni Sultan Suleyman Training and Research Hospital, Health Science University, 34303 Istanbul, Turkey

8Department of Emergency Medicine, Aksaray Training and Research Hospital, Aksaray University, 68200 Aksaray, Turkey

9College of Engineering and Technology, American University of the Middle East, 54200 Egaila, Kuwait

*Corresponding Author(s):murat.genc4@saglik.gov.tr (Murat Genç)

History Submitted: 17 March 2025 | Accepted: 27 May 2025 | Published: 08 December 2025
Copyright:  ©2025 The Author(s). Published by MRE Press.
This is an open access article under the CC BY 4.0 license (https://creativecommons.org/licenses/by/4.0/).

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Abstract

Background: Acute ischemic stroke (AIS) is a leading cause of mortality and morbidity worldwide. Cardiac electrical abnormalities, such as changes in the frontal QRS-T angle (fQRS-TA), are linked to adverse outcomes in various cardiovascular disorders. However, the prognostic significance of fQRS-TA in patients with AIS was not clearly established. This study aimed to evaluate the association between fQRS-TA and 30-day mortality in patients with AIS. Methods: This prospective, two-center observational study was conducted at Bilkent City Hospital and Etlik City Hospital between 01 June and 31 July, 2023. Patients aged ≥18 years diagnosed with AIS were enrolled, whereas individuals with hemorrhagic stroke, congenital heart disease, history of cerebrovascular events or significant electrocardiographic abnormalities were excluded. Baseline demographic data, clinical parameters, and electrocardiogram (ECG) findings were collected. fQRS-TA was defined as the absolute difference between the frontal plane QRS and T-wave axes. Patients were classified into survivors or deceased based on 30-day outcomes. Statistical analysis was performed using SPSS version 25. Results: The data of 85 AIS patients were assessed (mean age: 67.29 ± 12.88 years; 51.8% female), and the results demonstrated that fQRS-TA was significantly elevated in patients with hypertension and congestive heart failure (p < 0.05). A weak positive correlation was observed between age and fQRS-TA (p = 0.017), with the deceased group demonstrating significantly higher fQRS-TA values than the survivors (p = 0.045). The NIHSS (National Institutes of Health Stroke Scale) scores were also found to be significantly higher in the deceased group (p = 0.014). Conclusions: fQRS-TA is an easily obtainable ECG parameter that may serve as a predictor of short-term mortality in AIS patients. When combined with NIHSS scores, fQRS-TA may improve risk stratification and inform early clinical decision-making. Further large-scale, randomized studies are needed to confirm these findings.

Keywords:Ischemic stroke;Frontal QRS-T angle;Electrocardiography;Mortality prediction;NIHSS
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Cite this article

Murat Genç, Didem Çankaya Gökdere, Adil Emre Gezer, Melih Çamcı, Bensu Bulut, Medine Akkan Öz, Ramiz Yazıcı, Huseyin Mutlu, Zekeriya Uykan. Frontal QRS-T angle and mortality in ischemic stroke patients: a multicenter study. Signa Vitae. 2025; 21(12): 107-113. doi: 10.22514/sv.2025.194

1. Introduction

Ischemic stroke, the second leading cause of death and disability worldwide, is a major complication of cardiovascular disease and presents with clinical presentations ranging from transient ischemic attacks to extensive cerebral infarction [1, 2, 3]. In these patients, increased atherosclerotic burden and age-related myocardial fibrosis may influence cardiac conduction, contributing to increased mortality risks [4]. In addition, recent evidence suggests that acute ischemic stroke (AIS) can induce immediate adverse effects on cardiac function, including electrical disturbances [5, 6, 7], and these acute neurocardiogenic alterations have been linked to long-term outcomes in AIS patients [5, 6]. Given the five-year cumulative mortality rate, which ranges from 1% to 7%, early risk stratification and the development of appropriate therapeutic strategies remain essential [8].

During AIS, a cascade of neurochemical processes, referred to as the ischemic cascade, is initiated following the reduction in cerebral blood flow. This cascade involves excitotoxicity, oxidative stress, peri-infarct depolarizations, blood-brain barrier disruption, microvascular injury, altered hemostasis, inflammation and apoptosis. Although these processes evolve over several hours, they may continue for days even after achieving reperfusion. In line with previous findings, our study identified elevated serum troponin and urea levels, which may reflect systemic effects of the inflammatory response triggered by cerebral ischemia [7, 8, 9].

The ischemic core, the region of the brain directly surrounding the obstructed vessel, is usually the most severely damaged. Cellular necrosis in this area occurs rapidly through mechanisms such as lipolysis and proteolysis, making the tissue unsalvageable even despite prompt reperfusion [7, 8, 9, 10].

Electrocardiography (ECG) is a widely used, non-invasive diagnostic method for detecting cardiac electrical alterations in various clinical settings, including emergency and acute care units [9]. A standard 12-lead ECG provides multiple electrical parameters, including QT interval and ST segment changes, which have demonstrated prognostic relevance in cardiovascular morbidity and mortality [10, 11]. Among these parameters, the frontal QRS-T angle (fQRS-TA), defined as the absolute difference between the frontal plane QRS and T-wave axes, has emerged as a potential marker for mortality risk [9, 12]. Elevated fQRS-TA has been associated with increased mortality in conditions such as acute myocardial infarction, hypertension, coronary artery disease and malignant arrhythmias [12, 13, 14].

Given that AIS can lead to cardiac electrical abnormalities, it is plausible that fQRS-TA may also be affected. Therefore, this study aimed to assess changes in fQRS-TA among patients with AIS and to investigate its association with 30-day mortality.

2. Materials and methods

2.1 Study design and participants

This two-center, prospective observational study was conducted between 01 June 2023, and 31 July 2023, at Bilkent City Hospital and Etlik City Hospital, both located in Ankara, Türkiye. Bilkent City Hospital serves an average of 100,000 patients per month, while Etlik City Hospital serves an average of 120,000 patients monthly. Both institutions are designated comprehensive stroke centers. Ethical approval for this study was obtained from the Bilkent City Hospital Clinical Research Ethics Committee No. 2 (Approval Number: E2-23-4296), and the study was conducted following the principles outlined in the Declaration of Helsinki. This prospective study was conducted with the necessary institutional approvals, and informed consent was obtained from all participants.

Patients aged 18 years or older who were diagnosed with AIS in the emergency department were eligible for study inclusion. Exclusion criteria comprised a history of previous cerebrovascular incident (CVI), acute hemorrhagic stroke (AHI), congenital heart disease, acute or chronic infectious or inflammatory disease, pregnancy or lactation and chronic liver disease. Additionally, patients for whom NIHSS scores were not calculated, or ECGs were not recorded were excluded. Patients with complete or incomplete right or left bundle branch block, early repolarization, or ventricular hypertrophy on ECG were also excluded due to the potential confounding effects of these conditions on the fQRS-T angle.

2.2 Study protocol and data collection

Patients presenting to the emergency department with a diagnosis of AIS were initially assessed by an Emergency Medicine specialist or resident in either the red or yellow emergency triage areas. Simultaneously, physical examination, finger-stick blood glucose testing, ECG acquisition, and routine blood sampling were performed. The evaluating physician calculated and recorded the NIHSS score at the time of initial assessment. Once the patient was stabilized, non-contrast cranial computed tomography (CT) imaging was conducted. Patients with suspected AIS were quickly referred to neurology for consideration of thrombolysis or embolectomy to minimize treatment delays. AIS was defined in accordance with the American Heart Association/American Stroke Association (AHA/ASA) guidelines as follows [15]:

(a) acute symptom onset within 0–4.5 hours;

(b) presence of neurological deficits on physical examination;

(c) confirmation of ischemic stroke by cranial CT or magnetic resonance imaging (MRI); and

(d) exclusion of cerebral hemorrhage and non-vascular etiologies.

The AIS patients’ demographic, clinical, and laboratory data were retrieved from the hospital’s electronic medical records. The collected information included age, sex, history of chronic diseases, ECG parameters (such as QT, QRS, fQRS-TA), NIHSS score at admission, and the duration of hospitalization in both the general ward and intensive care unit (ICU). Based on 30-day follow-up outcomes, patients were classified into two groups: those who died from any cause within 30 days (deceased group) and those who survived (survivor group).

2.3 Electrocardiogram (ECG)

A standard 12-lead ECG was obtained and analyzed for each patient using a device with an acquisition rate of 25 mm/s and an amplitude scale of 10 mm/mV (Cardioline, Trento, Italy). The QRS and T axes were automatically calculated and reported by the ECG system. As described in previous studies, fQRS-TA was determined by calculating the absolute difference between the frontal plane QRS axis and the T-wave axis. For cases where the calculated value exceeded 180°, the fQRS-TA was determined using the formula: 360° − angle [16]. An example illustrating the use of the ECG device to determine fQRS-TA is presented in Fig. 1, where the section labeled “axes” displays the P, QRS and T axes sequentially.

Inclusion and exclusion criteria. CVD: cardiovascular disease.

Fig. 1.Inclusion and exclusion criteria. CVD: cardiovascular disease.

2.4 Statistical analysis

Statistical analysis was performed using SPSS version 25.0 (IBM Corp., Armonk, NY, USA). Descriptive statistics for categorical variables were presented as frequencies and percentages, while continuous variables were expressed as mean ± standard deviation (SD) or median with interquartile range (Q1–Q3), as appropriate. The distribution of continuous variables was assessed for normality. For comparisons between two independent groups, the Mann-Whitney U test was employed due to the non-normal distribution of dependent variables. Correlation analyses were conducted using Spearman’s rank correlation coefficient, as the variables did not meet the assumptions of normality.

3. Results

A total of 85 patients meeting the inclusion criteria from both centers were enrolled in the study. A flowchart of the study design and patient selection is shown in Fig. 2.

Using ECG device’s report to measure fQRS TA. HR: Heart Rate; PR: PR Interval; QRSd: QRS Duration; QT: QT Interval; QTC: Corrected QT Interval; QTcB: Interval Corrected by Bazett’s Formula; QTcF: Interval Corrected by Fridericia’s Formula; AVR: Augmented Vector Right; AVL: Augmented Vector Left; AVF: Augmented Vector Foot.

Fig. 2.Using ECG device’s report to measure fQRS TA. HR: Heart Rate; PR: PR Interval; QRSd: QRS Duration; QT: QT Interval; QTC: Corrected QT Interval; QTcB: Interval Corrected by Bazett’s Formula; QTcF: Interval Corrected by Fridericia’s Formula; AVR: Augmented Vector Right; AVL: Augmented Vector Left; AVF: Augmented Vector Foot.

The mean age of patients with AIS was 67.29 ± 12.88 years, and 51.8% (n = 44) were female. A weak positive correlation was observed between age and fQRS-TA (r = 0.259, p = 0.017). No significant correlation was identified between age and NIHSS score. Patients admitted to Bilkent City Hospital had significantly higher NIHSS scores compared to those admitted to Etlik City Hospital (p = 0.001). Additionally, fQRS-TA values were significantly higher in patients with a history of hypertension (HTN) and congestive heart failure (CHF) than in those without these conditions (p < 0.05). The comparison of fQRS-TA and NIHSS scores based on the sociodemographic and clinical characteristics of AIS patients is summarized in Table 1.

Table 1.QRS-T angle and NIHSS scores according to sociodemographic characteristics of the participants.
FeatureN (%)fQRS-TA (Q1–Q3)p valueNIHSS (Q1–Q3)p
Gender
Male41 (48.2)47.0 (17–120.5)0.651*4 (3–9.5)0.839*
Female44 (51.8)53.5 (29–128.75)4.5 (2–10.75)
Hospital
Etlik City61 (71.8)48.0 (18–125)0.369*3 (2–7)0.001*
Bilkent City24 (28.2)68.0 (36–126)7.5 (4.25–11.75)
HTN
Yes54 (63.5)66.5 (39.75–139.5)0.010*4 (2–8.5)0.967*
No31 (36.5)29.0 (18–72)4 (2–11)
DM
Yes34 (40.0)55.5 (29–131.25)0.650*4 (2–8.5)0.623*
No51 (60.0)53.0 (19–120)4 (2–10)
CAD
Yes21 (24.7)64.0 (18.5–1224)0.684*6 (3–10.5)0.191*
No64 (75.3)50.5 (24–127)4 (2–9.75)
CHF
Yes9 (10.6)138.0 (83–167.5)0.009*4 (1.5–6.5)0.377*
No76 (89.4)47.5 (20.25–99.75)4 (2–10)
HTN: High Blood Pressure; DM: Diabetes mellitus; CAD: Coronary artery disease; CHF: Congestive heart failure; fQRS-TA: Frontal QRS-T angle; NIHSS: National Institute of Health Stroke Scale; *: Mann Whitney-U test.

A weak positive correlation was identified between serum urea and troponin levels and fQRS-TA, while a moderate positive correlation was found between white blood cell (WBC)/neutrophil counts and NIHSS scores. These relationships between laboratory parameters and both fQRS-TA and NIHSS scores are presented in Table 2.

Table 2.QRS-T angle and NIHSS scores of participants according to laboratory findings.
FeatureMean ± SDfQRS-TAp valueNIHSSp value
Urea (mg/dL)47.19 ± 33.360.228*0.036−0.017*0.880
Creatine(mg/dL)1.08 ± 0.630.088*0.424−0.021*0.846
Sodium (mmol/L)139.11 ± 4.120.036*0.7460.194*0.075
Potassium (mmol/L)4.33 ± 0.490.064*0.5600.068*0.536
ALT (U/L)19.94 ± 10.720.031*0.7760.195*0.074
AST (U/L)23.87 ± 16.680.072*0.5110.139*0.205
Hb (g/dL)13.11 ± 2.15−0.122*0.2650.082*0.458
Plt260.88 ± 97.86−0.140*0.2030.078*0.475
WBC9.11 ± 2.74−0.138*0.2080.325*0.002
Neutrophile6.51 ± 2.78−0.058*0.5970.409*<0.001
Lymphocite1.74 ± 0.87−0.121*0.271−0.204*0.061
Troponine (ng/mL)33.33 ± 90.770.271*0.0120.070*0.526
CRP (mg/L)23.13 ± 45.510.186*0.1070.026*0.827
ALT: Alanin aminotransferase; AST: Aspartate transferase; Hb: Hemoglobin; Plt: Platelet; WBC: White blood count; CRP: C-reactive protein; SD: standard deviation; fQRS-TA: Frontal QRS-T angle; NIHSS: National Institute of Health Stroke Scale. *: Spearman correlation coefficient. The results in bold indicate statistically significant findings.

A positive correlation was also noted between fQRS-TA and NIHSS scores in patients with AIS, as shown in Table 3.

Table 3.Correlation analysis of QRS-T angle and NIHSS correlation coefficient.
NIHSS scorep value
QRS-T angle0.246*0.023
NIHSS: National Institute of Health Stroke Scale; *: Spearman correlation coefficient. The results in bold indicate statistically significant findings.

The median fQRS-TA in deceased patients was 92.5 (Interquartile Range (IQR): 36.5–154.75), significantly higher than the median value of 47 (IQR: 19–99) observed in survivors (p = 0.045). Similarly, the median NIHSS score was significantly higher in deceased patients (p = 0.014). The associations of fQRS-TA and NIHSS scores with 30-day mortality are detailed in Table 4.

Table 4.Evaluation of fQRS-T angle and NIHSS scores according to mortality.
MortalityN (%)fQRS-TA (Q1–Q3)p valueNIHSS (Q1–Q3)p value
(+)18 (21.2)92.50 (36.50–154.75)0.045*9 (3.75–14)0.014*
(–)67 (78.8)47 (19–99)4 (2–7)
fQRS-TA: Frontal QRS-T angle; NIHSS: National Institute of Health Stroke Scale; *: Mann Whitney-U test. The results in bold indicate statistically significant findings.

4. Discussion

In this study, fQRS-TA values were higher in patients with HTN, CHF and older age compared to those without these characteristics. Both fQRS-TA and NIHSS scores were significantly elevated in patients who died within 30 days, indicating that these parameters may be associated with short-term mortality in AIS. Moreover, we observed a positive correlation between fQRS-TA and NIHSS scores in patients with AIS (p = 0.023).

O’Donnell MJ et al. [17], in a large multicenter study involving cardiovascular disease (CVD) patients from 22 countries, reported that AIS frequently occurs at older ages and is commonly associated with comorbidities such as HTN, diabetes mellitus (DM) and atrial fibrillation (AF). Studies investigating the relationship between fQRS-TA and conditions such as coronary artery disease, CHF, and AF have found that elevated fQRS-TA is associated with older age [18, 19, 20]. Similarly, Tassone et al. [19] demonstrated a significant increase in fQRS-TA in patients with HTN, while Böyük et al. [20] reported a similar association in a case-control study examining elevated blood pressure. Consistent with these findings, our results indicated that fQRS-TA increased with age and was higher in AIS patients with HTN and CHF.

Becker et al. [21] showed that elevated high-sensitivity cardiac troponin (Hs-cTn) levels in AIS patients were often due to non-ischemic myocardial injury linked to the neurological event itself. In a separate study, Peng et al. [22] found that elevated blood urea nitrogen (BUN) levels, even within normal clinical limits, were associated with increased stroke risk and mortality. The onset of AIS initiates a cascade of neurochemical events, including excitotoxicity, oxidative stress, peri-infarct depolarizations, disruption of the blood-brain barrier, microvascular injury, hemostatic alterations, inflammation and apoptosis [23, 24]. These mechanisms may explain the elevations in biomarkers such as troponin and urea observed in our study. Additionally, AIS can affect cardiac metabolism and electrical activity by activating the central and autonomic nervous systems and alterations in neurohormonal pathways [25, 26]. As previously reported, AIS may induce various pathological ECG changes such as QT prolongation, U waves, biphasic T waves and ST segment deviations [8, 26]. Mboi et al. [27] emphasized that AIS is not merely a cerebral ischemic event but may also lead to systemic inflammatory responses and cardiac involvement, resulting in electrocardiographic alterations. Autonomic dysfunction following AIS may disrupt the cardiac conduction system and contribute to increases in fQRS-TA. Similar to these findings, our study demonstrated that fQRS-TA, as well as troponin and urea levels, were elevated in AIS patients and that fQRS-TA was positively correlated with these markers.

Fonarow et al. [28] identified a nearly linear association between increasing NIHSS scores and 30-day mortality in AIS patients. Consistent with this, our study found that NIHSS scores were significantly higher in the deceased group.

Gunduz et al. [29] reported that elevated fQRS-TA predicted in-hospital mortality and the need for mechanical ventilation in COVID-19 patients. Walsh et al. [30] showed that increased fQRS-TA was associated with adverse outcomes in coronary artery disease and could be used to predict mortality risk. In a large cohort study, Kors et al. [31] demonstrated that higher fQRS-TA was linked to increased 14-year mortality even in patients without established CVD. Similarly, Whang et al. [32] reported that increased fQRS-TA could predict adverse cardiovascular events and all-cause mortality. These findings support the notion that elevated fQRS-TA reflects a greater atherosclerotic burden. Given that AIS is a consequence of cerebral atherosclerosis, it could be reasonable to assume that increased fQRS-TA in AIS patients may reflect underlying vascular pathology. Usalp et al. [33] further reported that age-related atherosclerosis and fibrosis impair the cardiac conduction system, leading to increased fQRS-TA, arrhythmias and mortality [33]. In agreement with these studies, our findings suggest that elevated fQRS-TA in AIS patients is associated with higher NIHSS scores and increased short-term mortality.

The strengths of our study include its prospective design, the inclusion of two high-volume stroke centers, and the novel demonstration that fQRS-TA correlates with both NIHSS scores and 30-day mortality in AIS patients. However, several limitations must be acknowledged. First, the sample size was relatively small. Second, patients were not stratified according to treatment modality (e.g., thrombolysis, embolectomy), which may have influenced outcomes. Third, repeated fQRS-TA measurements were not performed. Lastly, due to limited classification of comorbidities, regression analysis for mortality could not be conducted, thereby limiting the ability to establish independent predictive value.

5. Conclusions

This study demonstrated that the fQRS-TA is an easily obtainable and potentially reliable electrocardiographic parameter for predicting short-term mortality in patients presenting to the emergency department with AIS. The integration of fQRS-TA with NIHSS scores may enhance early risk stratification and inform clinical decision-making in AIS management. Nevertheless, further large-scale randomized controlled trials are warranted to validate these findings and to establish the clinical utility of fQRS-TA in routine practice.

Availability of data and materials

Data used in the study will be made available by the author upon reasonable request.

Author contributions

MG, DÇG, MÇ—conceptualization, methodology; supervision. AEG, MÇ, ZU, MAÖ—data curation; formal analysis and drafting of the manuscript. MG, RY, MÇ—investigation; resources and critical revision of the manuscript. BB, MAÖ, ZU, AEG—data visualization and statistical analysis. MG, BB, RY, HM—literature review; writing—original draft preparation and editing. MG, MAÖ, RY, HM—validation; methodology and review of the final draft. All authors have read and agreed to the published version of the manuscript.

Ethics approval and consent to participate

Prior to the study, approval was obtained from Bilkent City Hospital Clinical Research Ethics Committee No. 2 (approval number: E2-23-4296) and the study was conducted in accordance with the tenets of the Declaration of Helsinki. Informed consent was obtained from all patients who participated in the study.

Acknowledgment

Not applicable.

Funding

This research received no external funding.

Conflict of interest

The authors declare no conflict of interest.

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